期刊
MICROBIOLOGYOPEN
卷 3, 期 1, 页码 15-28出版社
WILEY
DOI: 10.1002/mbo3.143
关键词
Acid resistance; Escherichia coli; RpoS; small noncoding RNA
类别
资金
- National Research Foundation of Korea (NRF) - Korea government (MSIP) [2010-0029167, 2011-0020322]
- Intelligent Synthetic Biology Center of Global Frontier - MSIP [2012M3A6A8054837]
- National Research Foundation of Korea [2010-0029167, 2011-0031944, 2011-0020322] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Escherichia coli and related enteric bacteria can survive under extreme acid stress condition at least for several hours. RpoS is a key factor for acid stress management in many enterobacteria. Although three rpoS-activating sRNAs, DsrA, RprA, and ArcZ, have been identified in E. coli, it remains unclear how these small RNA molecules participate in pathways leading to acid resistance (AR). Here, we showed that overexpression of ArcZ, DsrA, or RprA enhances AR in a RpoS-dependent manner. Mutant strains with deletion of any of three sRNA genes showed lowered AR, and deleting all three sRNA genes led to more severe defects in protecting against acid stress. Overexpression of any of the three sRNAs fully rescued the acid tolerance defects of the mutant strain lacking all three genes, suggesting that all three sRNAs perform the same function in activating RpoS required for AR. Notably, acid stress led to the induction of DsrA and RprA but not ArcZ.
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